Abstract
Atherosclerosis, a major contributor to vascular damage and plaque formation, is brought on by cellular senescence and chronic inflammation. A crucial matter that emerges is the classification of the disease in order to understand the pathogenic mechanisms before treatment. Given that oxidative stress, DNA damage, and inflammation contribute to cellular senescence, an increase in pro-inflammatory factors is detected in the atherosclerotic plaque, which exacerbates its instability while impeding vascular repair. This study emphasizes the importance of pathways such as Nrf2, ICAM-1, and p38 MAPK/p16(INK4A) in the development of atherosclerosis. It also underscores the potential of senescence-targeting interventions to complement the conventional treatments for atherosclerosis. The study promotes using senolytic approaches that may serve as effective adjuncts to conventional pharmacological treatments for atherosclerosis. Particularly, quercetin, a flavonoid, demonstrates a potential action as senolytic agent by mitigating macrophage senescence, improving lipid profiles, and reducing plaque size of up to 56% in experimental models. This review article advocates for integrating senolytic approaches, including nutraceuticals like quercetin and combination therapies, to improve cardiovascular health and age-related vascular disorders.